Krüpple like lactor 12 expression in colorectal cancer tissues and its relationship with epithelial mesenchymal transition

Abstract

Objective To explore the mechanism of krupple like lactor 12 (KLF12) in epithelial mesenchymal transition (EMT) of colorectal cancer. Methods Immunohistochemistry technique was utilized to detect the expression of KLF12, E-cadherin, N-cadherin, Vimentin and Snail in cancer tissues and adjacent mucosa tissues of 85 colorectal cancer patients, and clinical and follow-up data were also collected. KLF12-small interfering RNA (siRNA) was synthesized and transfected into HT-29 cells. Methyl thiazol tetrazolium (MTT) assay was applied to detect cell viability. Wound assay and Transwell assay were used to test invasion and migration of cells. The mRNA and protein expression of related genes was detected by real time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting, respectively. Results Results of immunohistochemistry demonstrated that the positive rate of KLF12, N-cadherin, Vimentin and Snail proteins in cancer tissues was higher, and that of E-cadherin was lower than that in adjacent mucosa tissues (χ2=43.724, 26.145, 35.788, 10.985, 59.225 respectively, P=0.000). The expression of KLF12 was associated with depth of tumors (χ2=7.773, P=0.005), and patients positive for KLF12 had poor prognosis (χ2=8.724, P=0.003). Strongest KLF12 protein was found in HT-29 cells (P=0.000). Cell viability, invasion and migration decreased after KLF12 was inhibited (F=22.541, 15.002 and 21.908 respectively, P=0.000). The expression of N-cadherin and Snail decreased, and E-cadherin increased after KLF12 was inhibited (P=0.000). Conclusion KLF12 might be involved in EMT of colorectal cancer to enhance invasion and metastasis. Key words: Kruppel-like transcription factor 12; Colorectal cancer; Epithelial mesenchymal transition; Invasion; Metastasis; Prognosis